ライフサイエンスコーパス: DVT

1 DVT affects most frequently the lower limbs and hence DV

2 DVT is a thromboinflammatory disorder developing largely

3 ntly higher FDG uptake than organized day 14 DVT (P=0.03).

4 hil depletion decreased FDG signals in day 2 DVT in comparison with controls (P=0.03).

5 ith a diagnosis of VTE that comprised 87,605 DVTs and 65,913 PEs (with and without DVT).

6 VT [3/184 (1.6%) vs 5/192 (2.6%); P = 0.72], DVT at 30 days (1.6% vs 3.6%; P = 0.34) or bleeding comp

7 or postthrombotic syndrome (PTS) after acute DVT.

8 diologists blinded for the presence of acute DVT and a third in case of disagreement.

9 c therapy for the initial treatment of acute DVT.

10 The majority of patients with acute DVT and a proportion of selected hemodynamically stable

11 ary embolism was induced 30 min or 2 d after DVT by intrajugular injection of a preformed blood clot

12 do not support routine wearing of ECS after DVT.

13 and PE but were 3- to 5-fold increased after DVT and 6- to 11-fold increased after PE when VTE was co

14 stockings are not routinely indicated after DVT, but are encouraged if there is persistent leg swell

15 n 25% to 50% of patients 3 to 6 months after DVT diagnosis.

16 Although 30-day mortality after DVT remained fairly constant over the last 3 decades, it

17 tion of lung emboli and venous thrombi after DVT-PE, revealing significant differences in uptake betw

18 atelets to the inferior vena cava wall after DVT induction were reduced in MC-deficient mice.

19 c deficiency in CLEC-2 are protected against DVT.

20 tion of NETs each confers protection against DVT amplification.

21 findings suggest that pulmonary embolism and DVT may not always have the same etiology, and encourage

22 Sex, DVT triggering event, and DVT resolution predicted LE-PTS in our cohort.

23 inolysis and decrease inflammation in PE and DVT patients, respectively, and offers insights into the

24 ions include imprecise definitions of PE and DVT.

25 1,119 with any PE, and 272 with both PE and DVT.

26 the risk for venous thromboembolism, PE, and DVT while increasing the risk for minor bleeding in pati

27 ET/computed tomography (CT) was performed at DVT time points of day 2, 4, 7, 14, or 2+16 (same-site r

28 Because DVT formation and resolution are associated with a prepo

29 fference was observed at least 5 days before DVT had developed.

30 ion was performed in a subset of mice before DVT formation and FDG-PET/CT.

31 scores >1; there was an interaction between DVT triggering event and sex.

32 Both DVT and IPI increased the activity of testosterone in a

33 RRs remained 25% to 40% increased after both DVT and PE but were 3- to 5-fold increased after DVT and

34 nticoagulation and those with a chronic calf DVT, a contraindication to anticoagulation, prior venous

35 dentified 697 patients with an isolated calf DVT and excluded 313 of these.

36 trasonographic detection of an isolated calf DVT from January 1, 2010, to December 31, 2013, at the V

37 0 days of the diagnosis of the isolated calf DVT.

38 oximal DVT or PE are low after isolated calf DVT.

39 d sonographically proven acute isolated calf DVT.

40 gnosis of a PE suspected at the time of calf DVT diagnosis were excluded.

41 oppler sonography for the evaluation of calf DVT may be limited by patient characteristics such as ob

42 The calf DVT involved an axial vein (anterior tibial, posterior t

43 signal decrease in both murine and clinical DVT.

44 eoperative IVC filter insertion demonstrated DVT rates of 0% to 20.8% and PE rates ranging from 0% to

45 essed in patients who subsequently developed DVT, compared to the patients without DVT.

46 compounds, (-)3,4-divanillyltetrahydrofuran (DVT), present in stinging nettle root extracts and used

47 ently been shown to boost coagulation during DVT, the underlying molecular mechanisms are not fully r

48 ory and prothrombotic lipid mediators during DVT progression in mice.

49 atients with cancer enrolled in the EINSTEIN-DVT and EINSTEIN-PE randomised controlled trials.

50 no cancer who were enrolled in the EINSTEIN-DVT and EINSTEIN-PE trials.

51 patients with deep-vein thrombosis (EINSTEIN-DVT) or pulmonary embolism (EINSTEIN-PE) were randomly a

52 deep vein thrombosis and pulmonary embolism (DVT-PE).

53 Deep Vein Thrombosis and pulmonary embolism (DVT/PE) is one of the most common causes of unexpected d

54 aged 18 to 70 years following the first-ever DVT.

55 MCs exacerbate DVT likely through endothelial activation and Weibel-Pal

56 sequently, D-dimer cannot be used to exclude DVT without an assessment of pretest probability.

57 ical study, 38 patients with lower extremity DVT or controls undergoing FDG-PET were analyzed.

58 ts with signs or symptoms of lower extremity DVT, such as swelling (71%) or a cramping or pulling dis

59 The FDG DVT signal in patients also exhibited a time-dependent d

60 d and validated for the diagnosis of a first DVT, no such well-defined strategies exist in the case o

61 In patients with cancer with a first DVT, treated for 6 months with LMWH, absence of RVT iden

62 30-year MRR was 1.55 (95% CI, 1.53-1.57) for DVT and 2.77 (95% CI, 2.74-2.81) for PE.

63 30-day MRR was 5.38 (95% CI, 5.00-5.80) for DVT and 80.87 (95% CI, 76.02-86.02) for PE.

64 target for an anti-inflammatory approach for DVT prophylaxis.

65 istones and neutrophil proteins critical for DVT development.

66 orting on the use of compression devices for DVT prevention.

67 Compression devices are often employed for DVT prophylaxis in these patients.

68 and are the only identified risk factor for DVT that can be ameliorated by physicians.

69 lity is the most significant risk factor for DVT, but a molecular and cellular basis for this link ha

70 tes for several established risk factors for DVT and pulmonary embolism separately.

71 apy as the only independent risk factors for DVT formation.

72 E in TPKA studies but less heterogeneity for DVT and pulmonary embolism in TPKA studies and for VTE,

73 was consistently 5- to 6-fold increased for DVT, whereas it improved for PE from 138 (95% CI, 125-15

74 , 0.20-5.9) patients with MRDTI negative for DVT and thrombophlebitis, who were not treated with any

75 VTE in all patients with MRDTI negative for DVT was 1.1% (95% CI, 0.13%-3.8%).

76 mboembolism (VTE) after a MRDTI negative for DVT.

77 rval [CI]: 0.33 to 0.75); increased risk for DVT (OR: 1.70; 95% CI: 1.17 to 2.48); nonsignificantly l

78 ositive test result on the basis of risk for DVT might improve the tradeoff between sensitivity and s

79 oxaparin prophylaxis in patients at risk for DVT should be optimized.

80 risk of subsequent PE, increase the risk for DVT, and have no significant effect on overall mortality

81 othelium provide the initiating stimulus for DVT development.

82 n and validate MCs as a potential target for DVT prevention.

83 cient for MCs were completely protected from DVT.

84 In general, DVT and PE patients require 3 months of treatment with a

85 estigated how many of these four vessels had DVT and compared them with respect to the pulsatility in

86 ts most frequently the lower limbs and hence DVT of the leg will be the focus of this article.

87 in mice, and at the site of origin of human DVT associated with fatal pulmonary embolism.

88 For iliofemoral DVT, QALY gains with PCDT were greater, yielding an incr

89 ermediate value in patients with iliofemoral DVT.

90 )Cu-FBP8 PET is a feasible approach to image DVT-PE and that radiogenic adverse health effects should

91 operative period is associated with imminent DVT, suggesting that it is a prothrombotic risk factor a

92 There was no change in DVT rates before and after CLOTS-1 (0.8% vs 1.0%).

93 There was no difference in DVT resolution (P = .41).

94 ality and are associated with an increase in DVT events.

95 to determine the role of mast cells (MCs) in DVT initiation and validate MCs as a potential target fo

96 Platelets play a role in DVT, but the impact of specific platelet receptors remai

97 d therefore that CLEC-2 might play a role in DVT.

98 at contributes to postthrombotic syndrome in DVT patients.

99 We established a stasis-induced DVT model in murine jugular veins and also a novel model

100 ients with symptomatic recurrent ipsilateral DVT (incompressibility of a different proximal venous se

101 DTI demonstrated acute recurrent ipsilateral DVT in 37 of 39 patients and was normal in all 42 patien

102 ole test for excluding recurrent ipsilateral DVT.

103 ically suspected acute recurrent ipsilateral DVT.

104 In conclusion, LR LE-DVT had more benign outcomes than Non-LR DVT.

105 We investigated the outcomes of LE-DVT in children.

106 non-neonates, respectively), of recurrent LE-DVT (P = .001; 10.7% and 2.0% in Non-LR and LRnon-neonat

107 ric lower extremity deep vein thrombosis (LE-DVT) can lead to postthrombotic syndrome (PTS) and other

108 and odds ratios (ORs) (and 95% CIs) of left DVT per 1% increase in percentage compression were calcu

109 ing compression was not associated with left DVT (adjusted ORs, 1.00, 0.99, 1.02) but above 70%, LCIV

110 LCIV compression may be associated with left DVT (adjusted ORs, 3.03, 0.91, 10.15).

111 ht DVT were more likely than those with left DVT to have a history of pulmonary embolism.

112 70% compression may be associated with left DVT.

113 one-fourth to one-half of all diagnosed leg DVTs.

114 DVT, LR DVT in neonates (LRneonates), and LR DVT in non-neonates (LRnon-neonates).

115 compared: non-line-related (Non-LR) DVT, LR DVT in neonates (LRneonates), and LR DVT in non-neonates

116 LE-DVT had more benign outcomes than Non-LR DVT.

117 ups were compared: non-line-related (Non-LR) DVT, LR DVT in neonates (LRneonates), and LR DVT in non-

118 METHODS AND In a mouse model, DVT was induced by partial ligation (stenosis) of the in

119 Here, using a murine DVT model of inferior vena cava (IVC) stenosis, we demon

120 il-dependent thrombus inflammation in murine DVT, and demonstrates a time-dependent signal decrease i

121 tion is set in motion leading to obstructive DVT formation.

122 s and myeloid leukocytes fostering occlusive DVT formation.

123 of postthrombotic syndrome in 25% to 60% of DVT patients.

124 ible for the initiation and amplification of DVT and for inducing its unique clinical features.

125 d for outpatient management of most cases of DVT in the acute phase.

126 raluminal fibrin formation characteristic of DVT.

127 The consequences of DVT include the development of postthrombotic syndrome i

128 type 9 (PCSK9) deficiency on development of DVT in mice.

129 biomarker within blood for the diagnosis of DVT/PE.

130 the detection of D-dimer to aid diagnosis of DVT/PE.

131 ts with active cancer and a first episode of DVT treated with low molecular weight heparin (LMWH) for

132 as associated with an increased incidence of DVT (OR = 1.83; 95% CI, 1.15-2.93, P-value = 0.01).

133 These findings support a mechanism of DVT pathogenesis in which loss of muscular activity resu

134 Thus, we propose a novel mechanism of DVT, whereby CLEC-2 and upregulation of podoplanin expre

135 Cellular mechanisms of DVT initiation remain poorly understood.

136 Mechanisms of DVT remain incompletely understood.

137 We describe a novel mouse model of DVT which reproduces a frequent trigger and resembles th

138 gical features, and clinical presentation of DVT in humans.

139 helial cells, and suggest that prevention of DVT and pulmonary embolism may be improved by mechanical

140 nsidered potential targets for prevention of DVT in humans.

141 TE rate was 0.96% (n = 13,809); the rates of DVT and PE were 0.71% (n = 10,198) and 0.33% (n = 4772),

142 trategies exist in the case of recurrence of DVT.

143 Recurrences of DVT were associated with faster formation (-9% lag phase

144 remodeling associated with the resolution of DVT.

145 ween plasma fibrinogen quintiles and risk of DVT alone (P-trend = 0.4).

146 rinogen is associated with increased risk of DVT alone, with any PE, and with PE in combination with

147 No increased risk of DVT was identified, nor any TEE reported in rhC1INH trea

148 There is an increased risk of DVT with surgery, particularly in patients who are not e

149 ory approaches to prophylaxis and therapy of DVT.

150 lmonary embolism, but little or no effect on DVT.

151 perative VTE, bleeding complications, and OP-DVT.

152 Eighteen patients (4.2%) had OP-DVT and were excluded.

153 The risk of OP-DVT is higher than that of perioperative DVT after color

154 r colorectal surgery and the incidence of OP-DVT remains unclear.

155 Those without OP-DVT were randomized to preoperative or postoperative CTP

156 ubjects with suspected pulmonary embolism or DVT and account for one-fourth to one-half of all diagno

157 se may not be causally associated with PE or DVT.

158 iants were not associated with risk of PE or DVT.

159 ned as D-dimer testing for all participants (DVT excluded at D-dimer levels <0.5 microg/mL).

160 OP-DVT is higher than that of perioperative DVT after colorectal surgery and preoperative screening

161 atio of $137 526/QALY; for femoral-popliteal DVT, standard therapy was an economically dominant strat

162 tive CTP with respect to early postoperative DVT [3/184 (1.6%) vs 5/192 (2.6%); P = 0.72], DVT at 30

163 h 23 (29%) were diagnosed with postoperative DVT.

164 lade body secretagogue from MCs, potentiated DVT in wild-type mice, and histamine restored thrombosis

165 ttent compression device designed to prevent DVT.

166 t intravascular abnormalities after previous DVT often hinder a diagnosis by compression ultrasonogra

167 all D-dimer assays or patients with previous DVT, study personnel were not blinded, and the trial was

168 e recurrent DVT at day 2 overlying a primary DVT at day 16).

169 nt proximal venous segment than at the prior DVT) and 42 asymptomatic patients with at least 6-month-

170 The sequence of events that promote DVT remains obscure, largely as a result of the lack of

171 Proximal DVT alone, higher C-reactive protein, D-dimer, peak thro

172 Proximal DVT occurred in 7 controls (5.0%) and 4 anticoagulation

173 Proximal DVT or PE within 180 days of the diagnosis of the isolat

174 randomized 692 patients with acute proximal DVT to PCDT plus anticoagulation (n=337) or standard tre

175 as PE (particularly if concomitant proximal DVT), a positive d-dimer test after stopping anticoagula

176 years to prevent PTS after a first proximal DVT in centres in Canada and the USA.

177 S did not prevent PTS after a first proximal DVT, hence our findings do not support routine wearing o

178 ssociated with a decreased risk for proximal DVT or PE at 180 days (odds ratio [OR], 0.34; 95% CI, 0.

179 onomically attractive treatment for proximal DVT.

180 Rates of proximal DVT or PE are low after isolated calf DVT.

181 resenting with a first symptomatic, proximal DVT were potentially eligible to participate.

182 definitely after a first unprovoked proximal DVT or PE is strengthened if the patient is male, the in

183 First unprovoked proximal DVT or PE may be treated for 3 to 6 months or indefinite

184 eg, cancer), or a second unprovoked proximal DVT or PE, is generally treated indefinitely.

185 y balanced after a first unprovoked proximal DVT or pulmonary embolism (PE).

186 for outpatients with low or moderate C-PTP (DVT excluded at D-dimer levels <1.0 microg/mL [low C-PTP

187 Recurrent DVT demonstrated significantly higher FDG uptake than or

188 Recurrent DVT was observed in 77 patients (25%; 6.6%/year) during

189 wn to accurately distinguish acute recurrent DVT from chronic thrombotic remains.

190 composite of centrally adjudicated recurrent DVT, fatal or nonfatal pulmonary embolism, and incidenta

191 ng strategy to accurately diagnose recurrent DVT.

192 r distinguishing acute ipsilateral recurrent DVT from 6-month-old chronic residual thrombi in the leg

193 6 min) were at the highest risk of recurrent DVT (odds ratio, 15.8; 95% confidence interval, 7.5-33.5

194 vidence regarding the treatment of recurrent DVT is sparse, in particular when it comes to deciding o

195 The baseline prevalence of recurrent DVT was 38%; superficial thrombophlebitis was diagnosed

196 for the diagnosis and treatment of recurrent DVT will be put forward.

197 Two typical cases of recurrent DVT, one with an unprovoked DVT and one with DVT during

198 d thereby improve the diagnosis of recurrent DVT.

199 ltered clot properties may predict recurrent DVT after anticoagulation withdrawal.

200 ced Ks and prolonged CLT predicted recurrent DVT.

201 ay 2, 4, 7, 14, or 2+16 (same-site recurrent DVT at day 2 overlying a primary DVT at day 16).

202 prevention of MC degranulation also reduced DVT.

203 Patients with right DVT were more likely than those with left DVT to have a

204 Sex, DVT triggering event, and DVT resolution predicted LE-PT

205 pression were not associated with left-sided DVT up to 70%; however, greater than 70% compression may

206 Stasis DVT demonstrated that the highest FDG signal occurred at

207 igation of the jugular vein to induce stasis DVT.

208 s and also a novel model of recurrent stasis DVT in mice.

209 neutrophils are indispensable for subsequent DVT propagation by binding factor XII (FXII) and by supp

210 when diagnosing a first episode of suspected DVT.

211 The pooled rates of symptomatic DVT were 0.63% (95% CI, 0.47%-0.78%) for knee arthroplas

212 is male, the index event was PE rather than DVT, and/or d-dimer testing is positive 1 month after st

213 Several lines of evidence indicate that DVT occurs at the intersection of dysregulated inflammat

214 ultivariable logistic regression showed that DVT pathogenesis and imaging-determined degree of thromb

215 Multivariable analysis showed that DVT resolution, triggering event, and sex predicted Modi

216 The DVT rate did not differ between trauma and general surge

217 postoperative day was more pronounced in the DVT patients with malignant versus benign brain tumors,

218 The DVTs occurred in 23.5% of patients who missed at least 1

219 casian man arrived with deep vein thrombosis DVT, pain, oedema and rubor of right lower limb and drug

220 RATIONALE: Deep vein thrombosis (DVT) and its complication pulmonary embolism have high m

221 lism (VTE), comprising deep vein thrombosis (DVT) and pulmonary embolism (PE), is a common, potential

222 lism (VTE), comprising deep vein thrombosis (DVT) and pulmonary embolism (PE), is a significant sourc

223 (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE), is the third most comm

224 her risk of developing deep vein thrombosis (DVT) and pulmonary embolism (PE).

225 Deep vein thrombosis (DVT) and pulmonary embolism are collectively known as ve

226 assessment of risk of deep vein thrombosis (DVT) by the Wells prediction rule were performed, and le

227 of recurrent same-site deep vein thrombosis (DVT) is a challenging clinical problem.

228 Deep vein thrombosis (DVT) is a common but unpredictable complication of surgi

229 Deep vein thrombosis (DVT) is a common cardiovascular disease with a major eff

230 Deep vein thrombosis (DVT) is a major cause of cardiovascular death.

231 ipsilateral recurrent deep vein thrombosis (DVT) is a major clinical challenge because differentiati

232 recurrent ipsilateral deep vein thrombosis (DVT) is challenging, because persistent intravascular ab

233 Deep-vein thrombosis (DVT) is regarded a chronic disease as it often recurs.

234 Deep vein thrombosis (DVT) isolated to the calf veins (distal to the popliteal

235 s with cancer who have deep vein thrombosis (DVT) of the lower limbs.

236 ly documented proximal deep vein thrombosis (DVT) or pulmonary embolism, with a life expectancy great

237 compression devices as deep vein thrombosis (DVT) prophylaxis methods in orthopedic and neurological

238 ium is widely used for deep vein thrombosis (DVT) prophylaxis, yet DVT rates remain high in the traum

239 es for lower extremity deep vein thrombosis (DVT) range from 88 to 112 per 100 000 person-years and i

240 learly higher risk for deep-vein thrombosis (DVT) than for pulmonary embolism.

241 Deep vein thrombosis (DVT) with its major complication, pulmonary embolism, is

242 Deep vein thrombosis (DVT), caused by alterations in venous homeostasis is the

243 ovoked isolated distal deep vein thrombosis (DVT), generally should be treated for 3 months.

244 isolated distal (calf) deep vein thrombosis (DVT), has a low risk of recurrence and is usually treate

245 In patients with acute deep vein thrombosis (DVT), pharmacomechanical catheter-directed thrombolysis

246 The rates of deep vein thrombosis (DVT), pulmonary embolism (PE), and VTE within 30 days of

247 can predict recurrent deep vein thrombosis (DVT), we studied 320 consecutive patients aged 18 to 70

248 ximal limb-threatening deep vein thrombosis (DVT).

249 tality, and subsequent deep vein thrombosis (DVT).

250 fter acute symptomatic deep vein thrombosis (DVT).

251 resolution of clots in deep vein thrombosis (DVT).

252 y approach to isolated calf vein thrombosis (DVT).

253 nitiating treatment of deep-vein thrombosis (DVT); in 8 patients, cancer was not known or suspected a

254 associated with both deep venous thrombosis (DVT) and its complication, pulmonary embolism (PE), and

255 ks for patients with deep venous thrombosis (DVT) and pulmonary embolism (PE) were markedly higher th

256 Deep venous thrombosis (DVT) and secondary pulmonary embolism cause approximatel

257 been associated with deep venous thrombosis (DVT) in the general population are risk factors for SLE

258 on the incidence of deep venous thrombosis (DVT) is controversial.

259 Deep venous thrombosis (DVT) is one of the most common cardiovascular diseases,

260 Deep venous thrombosis (DVT) remains a common and serious cardiovascular problem

261 d the association of deep venous thrombosis (DVT) with the presence of an IVC filter, accounting for

262 some complication of deep venous thrombosis (DVT).

263 cific for diagnosing deep venous thrombosis (DVT).

264 sion stockings (GCS) for deep vein thrombus (DVT) prophylaxis in acute stroke patients before and aft

265 ients were analyzed in 3 groups according to DVT pathogenesis and neonatal status: primary (G1), seco

266 s via glycoprotein Ibalpha and contribute to DVT progression by promoting leukocyte recruitment and s

267 ase, we found both pulmonary embolism due to DVT and paradoxical embolism due to existing patent fora

268 rt of children with objectively confirmed UE-DVT.

269 c UE-PTS frequency and severity depend on UE-DVT pathogenesis (primary/secondary) and, within the sec

270 ric upper extremity deep vein thrombosis (UE-DVT) and of UE postthrombotic syndrome (PTS) is still la

271 he pelvis prior to a diagnosis of unilateral DVT.

272 ses of recurrent DVT, one with an unprovoked DVT and one with DVT during anticoagulation, will be pre

273 monary embolism in TPKA studies and for VTE, DVT, and pulmonary embolism in TPHA studies.

274 analysts, and pooled incidence rates of VTE, DVT, and pulmonary embolism were estimated using random-

275 red separately to hospitalizations with VTE, DVT, or PE that had no corresponding comorbidities, cong

276 ed with a low pretest probability (ie, Wells DVT score <=1).

277 al cells surrounding the venous valve, where DVTs originate, express high levels of FOXC2 and PROX1,

278 by ~20-fold in the presence of zinc, whereas DVT binding was almost completely lost.

279 ately 41,944 in-hospital deaths (20,212 with DVT and 21,732 with PE) occurred among 770,137 hospitali

280 d male sex (75% vs 56%) were associated with DVT formation (P < .05 for all).

281 nd age 50 years or older are associated with DVT formation among trauma and general surgery patients.

282 d in vitamin K reduction and associated with DVT, correlate with SLE development in Asian subjects.

283 ith increased risk of PE in combination with DVT (P-trend < 0.0001): multivariable adjusted odds rati

284 ith increased risk of PE in combination with DVT but not with DVT alone.

285 with any PE, and with PE in combination with DVT.

286 Crystal structures of SHBG in complex with DVT or IPI at 1.71-1.80 angstrom resolutions revealed th

287 opulation, of whom 1,679 were diagnosed with DVT alone, 1,119 with any PE, and 272 with both PE and D

288 he proportion of patients not diagnosed with DVT during initial testing who had symptomatic venous th

289 ons with VTE and among hospitalizations with DVT or PE.

290 k of PE in combination with DVT but not with DVT alone.

291 ly occurred for IPI-bound SHBG, but not with DVT-bound SHBG.

292 DVT, one with an unprovoked DVT and one with DVT during anticoagulation, will be presented.

293 ite such therapy, up to 50% of patients with DVT develop postthrombotic syndrome, and up to 4% of pat

294 al evaluation and treatment of patients with DVT.

295 to accelerate this process in patients with DVT.

296 d 1.9 (95% CI, 1.0-3.6) for PE in those with DVT (P-trend = 0.003).

297 spitalizations with VTE and among those with DVT or PE.

298 87,605 DVTs and 65,913 PEs (with and without DVT).

299 eloped DVT, compared to the patients without DVT.

300 deep vein thrombosis (DVT) prophylaxis, yet DVT rates remain high in the trauma and general surgery